The present study seeks to provide answers to questions regarding the neural control of the larynx during phonation in monkeys. Anatomical and physiological evidence indicates two descending pathways that may be important in phonation, converge at the periaqueductal gray(PG) of the midbrain. Projection from the anterior cingulate gyrus (CG) to the PG are known to be important for phonation, whereas projections from the motor cortex influence laryngeal muscles but have not been shown to affect phonation. Pilot data utilized microstimulation of the motor cortex and wide-field stimulation of the PG. Stimulation of the PG elicited phonation, and of the motor cortex affected laryngeal muscle activity. Simultaneous stimulation of the two structures sometimes interacted but the site and mechanisms of this interaction are unknown. I propose to study these mechanisms of laryngeal control by the method of chronic single unit recording in awake monkeys. Monkeys will be prepared for chronic single unit recording using standard aseptic surgical techniques. A recording chamber will be placed so as to allow recording of single PG neurons. Chronic stimulation electrodes will be implanted in the CG and laryngeal motor cortex. Chronic EMG electrodes will be implanted in the laryngeal muscles. In the first study the CG will be stimulated to elicit phonation. Temporal correlations between CG stimulation and PG unit activity will be sought. The motor cortex will then be stimualted to assess any changes in PG or EMG activity or acoustical properties of phonation. The second study will involve training monkeys to vocalize and PG unit activity will be recorded during such vocalizations. Temporal and spatial (pitch and intensity) correlations between phonation, PG activity and laryngeal EMG will attempt to determine in what ways the PG units are involved in phonation. Data from this study will contribute to a better understanding of the nature of neural control over features of phonation such as pitch and intensity control. It is also hoped that these data may eventually lead to improved theories on the etiology of neurogenic voices disorders such as spastic dysphonia.